Seeing Clearly: How Prozac Restores Function to the Brain

There’s major news on the antidepressant front, but it comes in an odd form: research on treating “lazy eyes” in rats. A study suggests that, yes, Prozac and similar medicines really do make the brain more flexible.

The report, titled “The Antidepressant Fluoxetine Restores Plasticity in the Adult Visual Cortex,” appears in the current issue of Science. It tests the hypothesis, current for some time now, that drugs like Prozac work through stimulating factors in the brain that allow nerve cells there to grow and make new connections. If that theory holds, then perhaps the medications might allow the adult mammalian brain to take on some of the “plasticity,” or capacity for adaptive change, normally present only early in development.

The researchers, José Fernando Maya Vetencourt of the Scuola Normale Superiore in Pisa, Italy, and colleagues elsewhere in Europe, began by depriving rats of the use of one eye by sewing it shut. Over time, the visually-deprived rats came to rely solely on the working eye and lost the capacity for binocular vision even when both eyes were again open.

Students of the history of medicine will be reminded of the experiments that won David H. Hubel and Torsten Wiesel the Nobel Prize 1981. Using cats, Hubel and Wiesel showed that the brain development necessary for vision in a given eye results from the use of that eye during a critical period of development in infancy and childhood. Amblyopia, or partial blindness in one eye, is a disorder not of the eye but of the brain. Rats have a similar critical period. By the fifty-fifth day of life, they lose the ability to change the way the brain handles vision.

Maya Vetencourt did two sets of experiments, one with rats subjected to temporary visual deprivation and one with rats made amblyopic over the long term. In both cases, the rats remained blind in one eye — except that in rats treated chronically with Prozac, normal vision returned. The recovery had nothing to do with drug effects on the eye. The medication had stimulated BDNF, or brain-derived neurotrophic factor, and the relevant part of the brain had become active again, elaborating new cells and new cell pathways. The stimulation of BDNF probably took place via serotonin, the neurotransmitter that Prozac effects most directly. Another transmitter, GABA, may also have been involved.

Interestingly, “environmental enrichment,” providing the rats with more stimulation and opportunity to explore, also improved vision, possibly through stimulating serotonin and thus BDNF. In the rat literature, environmental enrichment has overtones of psychotherapy, exercise, and good social support — factors that in humans can mitigate depression.

The researchers point to evidence that antidepressants restore adaptability in the human brain. They conclude: “a similar increase in plasticity, which is here described in the rodent visual cortex, may also take place in the human visual system, during chronic SSRI treatment” That is, Prozac may help in the treatment of “lazy eye” in adult humans. The authors add: “Our results open the possibility that chronic treatment with antidepressants may also have similar effects in other brain areas, such as those involved in mood regulation in depressed patients . . .” SSRIs may also help to treat other neurological systems where recovery depends on a renewed capacity for making nerve call connections in the brain.

These experiments serve as further — and quite dramatic — evidence in favor of the current theories of depression and of antidepressant action, the ones I consider in detail in Against Depression. By this account, recovery from mood disorder turns on the brain’s ability to make new nerve cells and then elaborate working connections between these cells. Many studies have pointed in the direction of the first part of this model: antidepressants do seem to protect and restore the brain’s ability to make neurons. This new work with “lazy eye” speaks to the second part: those new neurons can function and restore lost capacities to the injured animal.

I have written often of the worries every doctor must have about long-term use of antidepressants. There may be hidden negative effects. A growing body of research points in a different direction: the medications may confer unexplored benefits as well.

Whether or not the long term use of antidepressants eventually causes health problems, those of us who have had multiple episodes of severe depression (and have been hospitalized for depression) would almost certainly have greatly shortened lives without the protection of antidepressants every day for the rest of our lives. In some ways, it is like questioning the long term use of insulin for diabetics. Even maintenance doses of antidepressants do not prevent future episodes for many of us, but the frequency of those episodes are greatly reduced and it becomes possible for many of us to have normal and, yes, even happy lives for the most part.

A normal, healthy brain will respond to the stress placed on it by receptor blocking chemicals by generating additional receptors--which is in fact why cold turkey withdrawal is such a bad move, and why even slow withdrawal is for most people painful and difficult to the point, for many, of being nearly impossible.

To say "Gee! Good news! Turns out we're only making your brain more flexible!" describing studies like these as good "news" is self-serving, misleading, ad hoc, nauseating and frightening.

77 year old male. High functioning as a psychotherapist. Began prozac within two years of it coming out, 1988 (+-) for post Vietnam PTSD type andogenous depression. If I go off, depression returns. Tested that a few times early on, but now continue 40mg daily. I do wonder at times of the long term effects, etc., but as one man said, it is like asking of the long term effects of insulin on diabetics (funny).
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